1. Field of the Invention
This invention relates to a method and device for the treatment of hypertrophic cardiomyopathy. More specifically, this invention relates to a method and device that retracts the thickened myocardium.
2. Description of the Prior Art
Hypertrophic cardiomyopathy (HCM) is a complex type of heart disease that affects the heart muscle. It causes thickening of the heart muscle (especially the ventricles, or lower heart chambers), left ventricular stiffness, mitral valve changes, and cellular changes.
Thickening of the heart muscle (myocardium) occurs most commonly at the septum. The septum is the muscular wall that separates the left and right side of the heart. Problems occur when the septum between the heart's lower chambers, or ventricles, is thickened. The thickened septum may cause a narrowing that can block or reduce the blood flow from the left ventricle to the aorta—a condition called “outflow tract obstruction.” The ventricles must pump harder to overcome the narrowing or blockage. This type of hypertrophic cardiomyopathy may be called hypertrophic obstructive cardiomyopathy (HOCM).
HCM may also cause thickening in other parts of the heart muscle, such as the bottom of the heart called the apex, right ventricle, or throughout the entire left ventricle.
Stiffness in the left ventricle occurs as a result of cellular changes that occur in the heart muscle when it thickens. The left ventricle is unable to relax normally and fill with blood. Since there is less blood at the end of filling, there is less oxygen-rich blood pumped to the organs and muscles. The stiffness in the left ventricle causes pressure to increase inside the heart.
The narrowing of the left ventricular outflow tract disrupts the proper function of the mitral valve, resulting in outflow obstruction and increased pressure in the left ventricle. The obstruction is the result of the mitral valve striking the septum. When this occurs, the mitral valve frequently leaks, causing the blood to go back into the left atrium.
HCM is a genetic disease with an autosomal dominant pattern of inheritance and affects an estimated 600,000 to 1.5 million Americans, or one in 500 people. This disease entity carries annual rates of heart failure, death, or transplantation of 0.55% and stroke-related deaths of 0.07%. HCM is the most common cause of sudden cardiac death in people under the age of 30.
Symptoms associated with the presence of ventricular tachycardia or heart failure include chest pain, shortness of breath and fatigue, syncope, and palpitation.
Regardless of the presence of symptoms, significant outflow tract obstruction at rest is an independent predictor of poor prognosis in patients with HCM. After adjusting for age, gender, heart failure at entry, presence of atrial fibrillation, and LV wall thickness ≧30 mm, patients with obstruction had a high rate of HCM-related mortality (relative risk 1.6, 95% CI 1.1-2.4).
Patients with obstructive HCM who are severely symptomatic (e.g., New York Heart Association functional class III or IV) or have recurrent syncope despite pharmacologic therapy are candidates for cardiac surgery called septal myectomy. During this surgical procedure, the surgeon removes a small amount of the thickened septal wall (approximately 3 to 15 g) to widen the outflow tract (the path the blood takes) from the left ventricle to the aorta. Myectomy is considered when medications are not effective in treating HCM. Peri-operative mortality varies from 0.7-6.0%. Excessive resection of muscle can cause a ventricular septal defect, a serious complication that may occur in up to 2% of patients. Other complications include inadequate intraoperative protection of the hypertrophied muscle against ischemia, causing LV dysfunction at a later date, damage to the aortic valve, causing aortic regurgitation subsequently requiring aortic valve replacement, and development of left bundle branch block (LBBB) or complete heart block (CHB) requiring a permanent pacemaker which occurs postoperatively in approximately 5 to 10% of patients.
Nonsurgical septal reduction therapy (NSRT), also called transcoronary ablation of septal hypertrophy (TASH) or ethanol septal ablation, consists of infarction and thinning of the proximal interventricular septum via infusion of ethanol into the first septal perforating branch of the left anterior descending coronary artery through an angioplasty catheter thereby reducing the size of the septum. Ethanol septal ablation in patients with HCM has been complicated by ECG changes, including transient QT prolongation, Q waves, right bundle branch block, and complete heart block (14-25%). Other more serious complications include ventricular tachyarrhythmias, arrhythmic death, and, although infrequent when performed by experienced operators, a large myocardial infarction caused by escape of ethanol from the target vessel. Another concern has been that subsequent scarring might increase the long-term incidence of ventricular arrhythmias, bradyarrhythmias, and heart failure.
It is therefore an objective of the present invention to eliminate the need for invasive septal myectomy surgery and the significant morbidity and mortality associated with open heart surgery complications, such as temporarily stopping blood flow through the heart.
It is yet another objective of the present invention to eliminate the serious and lethal complications of noninvasive septal ablation done via catheters.